• GBS is seen in a higher-than-expected rate in patients with sarcoidosis, systemic lupus erythematosis, lymphoma, HIV infection, Lyme disease, and solid tumors.
• Complications include respiratory failure, autonomic disturbances, aspiration, fluid balance and nutritional deficiencies, deep venous thrombosis, infection susceptibility, muscle atrophy, and joint contractures.

• Myasthenia gravis
• Botulism
• Intoxication (heavy metals, organophosphates, etc.)
• Myopathy
• Poliomyelitis and other acute (viral) motor neuron dieases
• Acute cerebellar ataxia
• Transverse myelitis
• Chronic inflammatory demyelinating polyneuropathy (CIDP)
• Vasculitic neuropathy
• Diphtheric neuropathy (rare)
• Porphyric neuropathy
• Locked-in state
• Psychogenic

Question: Problems walking?
Significance: Most patients first note leg weakness or gait instability that progresses over days to weeks.

Question: Diminished finger and toe sensation?
Significance: Parasthesias and pain frequently appear early in the course.

Question: Respiratory problems?
Significance: Weakness may interfere with breathing.

Finding: Deep tendon reflexes are lost.
Significance: Typical sign of GBS.

Finding: Facial weakness
Significance: Occurs in many cases, and respiratory failure dictates intubation in up to 10% of patients.

Finding: “Floppy infant”
Significance: Neonates and infants may present as floppy infants.

Test: Lumbar puncture
Significance: Nearly all patients, particularly children, have elevated cerebrospinal fluid protein with minimal pleocytosis (<50 WBC/mm³).

Test: Electrodiagnosis
Significance: Often helpful when clinical/cerebrospinal fluid findings are ambiguous. Evidence of demyelinating neuropathy is in clinically affected areas. Slowing of motor conduction, motor conduction block, prolonged distal motor latencies, temporal dispersion of motor responses, and abnormalities of F waves are the electrodiagnostic features of demyelinating neuropathy.

Test: In atypical cases, consider heavy metal screen, HIV titer, Lyme titer, porphyria screen, acetylcholine receptor antibodies.
Significance: See Differential Diagnosis.

• Plasma exchange is the primary therapy for GBSA. Total plasma exchange volume of 200 to 250 mL/kg divided in three to five treatments over 7 to 14 days, beginning within 30 days of the onset of weakness significantly hastens recovery in GBS. Plasma exchange has not been studied in large trials in children, but its use in children is widespread and it is well tolerated.
• Intravenous immunoglobulin (IVIG) has been tried with success in adults and children. One large study showed it to be of equivalent efficacy to plasma exchange in adults. Many investigators have reported an increased rate of relapse in patients treated with IVIG. A trial comparing IVIG with plasma exchange in adults is nearly complete, and a similar trial in children is planned.
• Corticosteroids have not been shown to be helpful and generally not used.
• Management in an intensive care unit is usually required. Respiratory vital capacity should be frequently monitored and elective intubation performed when the vital capacity falls below 10 mL/kg. Particular attention should be given to preventing secondary pressure neuropathies.
• Pain is common in GBS and should be treated aggressively.
• Prevention measures are not known.

• First improvement typically begins 2 to 3 weeks after onset of symptoms but may not occur for 1 to 2 months in some patients.
• Improvement continues for 1 to 2 years.

• Respiratory failure may occur quickly.
• Approximately 10% of patients present with a variant syndrome—pure motor GBS, pharyngeal-cervical-brachial weakness, paraparetic form, ataxic form or Fisher syndrome (ophthalmoplegia, ataxia, and arreflexia).
• Many patients appear to have psychogenic instability early in the course of GBS

Q: Is GBS contagious?
A: No.

Q: Will I get GBS again?
A: Acute relapses occur in 1% to 5% of patients in large series. CIDP can rarely begin with a rapid onset of weakness indistinguishable from GBS.